Dolanbay, Elif GelenliMert, TugayBender, Gozde CaliskanBektas, HavaUslu, UnalFernandez-Rodriguez, Claudio EnriqueDasdag, Suleyman2025-11-302025-11-3020250077-89231749-663210.1111/nyas.701162-s2.0-105019496771https://doi.org/10.1111/nyas.70116https://hdl.handle.net/20.500.14720/29075This study investigates the long-term effects of prenatal exposure to 3.5 GHz radiofrequency radiation (RFR) on male reproductive health. Pregnant Wistar Hannover rats were divided into sham control, full-gestation exposure (3T RFR), and late-gestation exposure (2T RFR) groups (2 h/day). Male offspring were euthanized at 12 months for testicular analysis. In the 3T RFR group, seminiferous tubule diameter and epithelial height were significantly reduced compared to controls (adjusted p = 0.03 and 9.71 x 10-8), along with lower Johnsen scores (adjusted p = 0.022). Abnormal sperm morphology increased significantly (adjusted p = 0.036). gamma-H2AX immunostaining scores were elevated in the 2T and 3T groups (adjusted p = 0.012 and 6.36 x 10-9). Beclin-1 expression was significantly higher in the 3T group versus sham and 2T groups (adjusted p = 8.55 x 10-4 and 4.51 x 10-6). TUNEL-positive cell counts were significantly higher in both RFR groups than in sham (adjusted p = 8.77 x 10-18 for 3T, 6.42 x 10-17 for 2T), as was the apoptosis index (adjusted p = 8.77 x 10-18 for 3T, 5.66 x 10-17 for 2T). All p values were Holm-Bonferroni corrected. These findings indicate that prenatal exposure to 3.5 GHz RFR results in persistent testicular damage, impaired spermatogenesis, and increased DNA damage, autophagy, and apoptosis in adult male rats.eninfo:eu-repo/semantics/openAccess3.5 GHz RFRAutophagyDNA DamagePrenatal ExposureSperm MorphologyTestisArticle